Discover and read the best of Twitter Threads about #inflammatory

Most recents (16)

In the endothelium,selective impairment of insulin-mediated NO production may contribute to the development of #hypertension, endothelial dysfunction, atherogenesis, insulin resistance. NO induces vasodilation and inhibits platelet aggregation, vascular smooth muscle cell growth
Angiotensin #Ang2 inhibits insulin-mediated PI3K pathway activation, thereby impairing endothelial NO production and Glut-4 translocation in insulin-sensitive tissues, which results in vascular and systemic insulin resistance, respectively.
On the other hand, Ang II enhances insulin-mediated activation of the mitogen-activated protein kinase (#MAPK) pathway, which leads to vasoconstriction and pathologic vascular cellular growth.
Read 14 tweets
#location location location: thrilled to share our work @CellCellPress! #interferons dictate #COVID19 severity! Specific #IFNs are produced along the #airways in response to #SARSCoV2 and drive protective or detrimental #transcriptional programs! 1/7 doi.org/10.1016/j.cell…
IFNs are driven by high #viral #loads, suggesting that viral recognition is only achieved when #SARSCoV2 reaches a certain threshold! Efficient induction of protective IFNs is preferentially achieved by younger patients, further explaining susceptibility of elders to #COVID19 2/7
#IFNL1 & #IFNL3 characterize mild illness & drive potent anti-#SARSCoV2 #ISGs in the upper #airways. Severe patients show #typeI IFN & #IFNL2 along the respiratory tract but lack ISGs, dampen cell proliferation programs associated to #repair and boost #apoptotic #p53 pathways 3/7
Read 7 tweets
In a meeting I watched today, microglia priming was mentioned in #LongCovid and #ME/CFS. It’s important to clarify what “microglia priming” means. Microglial priming does not mean that after a trigger has “cleared” microglia remain perpetually activated
2/ Instead, microglia priming goes like this 👉 When microglia or other glial cells detect #infection, injury, or inflammatory mediators, they enter a state of activation in which they change morphology and release their own neuroexcitatory inflammatory mediators
3/ Then, after activating, they retain a “primed” functional state which causes an even more robust response to *subsequent* infectious/immune/#inflammatory challenges. And as cells, microglia live long lives (they are not replaced as often as many other cell types)
Read 13 tweets
Dear Twitter, Last night I slept from just after midnight to just after 6AM, AND from 07:24-10:24AM. I guess my brain was REALLY keen on 2x90-miN sleep cycles, bc my narcoleptic phone turned itself off & I woke up w/o my alarm!Here’s me better-rested than I’ve been in ages. A fairly close-up shot of m...
Apparently my good night’s sleep has yet to restore my powers of Superior Proofreading, however. 🙄😆
Whew! Washed & dressed, had quick food+drugs, livetweeted HPS seminar on gender in the academic field of finance research (presented by #CordeliaFine), listened to voicemail, folded laundry while waiting for @steve_kambouris to get off a work call...
Read 11 tweets
Pedersen, N., Duricova, D., & Munkholm, P. (2009). Pulmonary Crohn's disease: A rare extra-intestinal manifestation treated with infliximab. Journal of Crohn's & colitis, 3(3), 207–211. doi.org/10.1016/j.croh…
Hayek, A. J., Pfanner, T. P., & White, H. D. (2015). Inflammatory bowel disease of the lung: The role of infliximab?. Respiratory medicine case reports, 15, 85–88. doi.org/10.1016/j.rmcr…
Read 10 tweets
Dear #NEISvoid/twitter, I am VINDICATED (&, uh, still hyper on steroids, FWIW). Awesome Sleep/RespDoc is of the educated &firm opinion (upon reviewing my hospital discharge summary, lung function test results...which the hospital still hadn’t passed on yet as of this morning? 🙄)
...that I have NOT suddenly & completely coincidentally managed to develop asthma for the first time in my life at the tender age of 39 (although he thinks it does sound like a bronchospasm cough, which is literally how I was describing it when it first started happening.
Nor do I seem to have any kind of lung problem, nor a recent past upper/lower resp tract infection). Although apparently he hadn’t received the results of either of the sputum culture tests from the hosp. I’m assuming they were boringly negative or I’d have heard by now, though.)
Read 37 tweets
1/ THREAD 7: Viral Latency and a Hematogenous Route to CNS?

Is it even conceivable that #SARSCoV2 could establish latency in sensory ganglia (like trigeminal ganglia in HSV1) and reactivate to cause recurrent disease as respiratory droplets could enter the eyes, nose, and mouth?
2/ Specifically, talking about the peripheral nerves of the eyes, nose and mouth here. And thinking along the lines of why clinicians are seeing the loss of smell and altered taste in so many patients. Please remember, I am not a #virologist or an infectious disease specialist!
3/ HYPOSMIA DATA:
Both the American Academy of Otolaryngology - Head and Neck Surgery AAO-HNS and ENTUK have classified loss of smell and altered taste as significant symptoms in #COVID19. #Covid19UK

entnet.org/content/corona…

entuk.org/sites/default/…
Read 22 tweets
(1/n) Delighted to share our work using #scRNAseq to explore the intersection between regeneration, development and #immune recognition in #cancer #metastasis online @NatureMedicine @sloan_kettering @WeillCornell @scell_papers @dana_peer @LabMassague
nature.com/articles/s4159…
@NatureMedicine @sloan_kettering @WeillCornell @scell_papers @dana_peer @LabMassague (2/n) human primary #lungcancer is characterized by the emergence of regenerative cell types, typically seen in response to lung injury, but showing striking lineage promiscuity (identity confused!)
@NatureMedicine @sloan_kettering @WeillCornell @scell_papers @dana_peer @LabMassague (3/n) #metastasis exhibits a continuum of more primitive stem to epithelial progenitor states – driven in large part by key embryonic and lung-specifying transcription factors, SOX2 and SOX9.
Read 11 tweets
#Antisemitic incident!

#Italy #Mailand #Milan
The 89-year-old Milanese Liliena Serge is a #Holocaust #survivor. In January 1944, at the age of 13, she came to #Auschwitz with her father. Unfortunately, her father did not surrive.
She is now traveling all over #Italy to tell her story, and has even been voted a life #senator in gratitude for her work. But for months, the #Auschwitz survivor Liliana Segre gets Daily Hundreds of hate messages,
death threats and #antiSemitic #inflammatory messages that she is now under permanent #police protection. Yesterday, 5000 Denonstranten met on track 23 in #Milan. (The track for transport to #Auschwitz) At the monument, people met to express their solidarity with the survivors.
Read 4 tweets
And just today this new study further challenges the sterile #placenta! 👉 This team identified R. insidiosa as a bona fide resident at the placental basal plate..by using species-specific FISH probes to confirm + localize R. insidiosa within basal plate tissue specimens at term
1/1 From paper 👉 “We show that R. insidiosa is a bona fide resident in human #placental basal plate. It can access trophoblast cells in culture and within basal plate tissues where it localizes to intracellular single-membrane vacuoles and can replicate...”
2/2 “...However, the presence of R. insidiosa does not cause cell death and does not induce a pro-#inflammatory immune response suggesting that it is not harmful in and of itself...”
Read 5 tweets
This! The activity of the host #immune response largely determines whether #pathobionts acquired from an #FMT donor might become capable of virulence 👉 So including immune status in the study of FMT outcomes would be extremely informative
IMO immune status should be included in the general study of #antibiotic resistant infection 👉 It’s no coincidence that most “superbug” infections occur in immunocompromised patients, often in hospitals (w/ patients on cocktails of steroids for procedures like organ transplants)
Because extrapolate that trend and consider that the immunosuppressive biologics used to palliate “#autoimmune” disease symptoms are the top selling medications in the world 👉 With top side effects of such drugs being “serious #infection by viruses, fungi or bacteria”(see below) Image
Read 6 tweets
Nice work @drmfreire + team at @JCVenterInst! 👉 They found that local #periodontal pathogen enrichment was positively associated with high systemic inflammatory profiles in patients with Systemic #Lupus Erythematosus: biorxiv.org/content/10.110… ImageImageImageImage
Quote from paper 👉 “...the gut #microbiome, and recently the #oral microbiome, showed direct impact on SLE subjects, the complexity of chronic diseases such as #SLE is beyond isolated body compartments, and it requires the integration of host-microbial interactions.”
Also 👉 “At the center of #autoimmune pathogenesis, this study provides evidence that #inflammatory response to #microbiome controls the severity, and magnitude of the #SLE disease”
Read 4 tweets
“Missing #microbes” are a factor in the development of chronic #inflammatory disease 👉 But personally, I’m more concerned about the fact that many aspects of modern living are driving a rise in “missing #immunity” and the consequent survival of “additional persistent #pathogens
Here’s an example 👉 #Formula feeding is often associated w/ increased chronic #disease incidence☝️ Meanwhile, #breast milk has a #microbiome, but is ALSO filled w/ antimicrobial compounds + metabolites that play a key role in the immune’s system’s ability to manage #infection
This team found that interactions b/t neonatal #saliva and #breast milk released #antimicrobial compounds including H202☝️These compounds inhibited growth of a range of human pathogens: nature.com/articles/s4159… ImageImageImage
Read 8 tweets
Interesting! 👉 But we may never find that holy grail (a common #microbiome dysbiosis tied to specific inflammatory conditions)☝️B/c the microbiome is so vast..that the metabolic dysfunction driven by different #organisms can result in similar clusters of #inflammatory symptoms
Yet we can still use/develop treatments based off “big picture” trends 👉 Eg: no two patients w/ #cancer have the same #tumor mutations☝️But #immununotherapy harnesses the broad potential of activated T cells to target tumors (w/ therapy “details” personalized per #patient)
Plus we’ve already established many common features of #microbiome dysbiosis 👉 KEY being the the ability of #microbes + #viruses to create proteins/metabolites that dysregulate human signaling pathways☝️Good example here: nature.com/articles/s4156… ImageImage
Read 4 tweets
Why is the future of chronic #inflammatory disease #polymicrobial (organisms interacting)? 👉 This paper describes how even in #Lyme Neuroborreliosis, different strains of Borrelia often persist in a #biofilm, or community-based form: frontiersin.org/articles/10.33… ImageImageImageImage
The ability of Borrelia to form into #biofilm communities may 👉 “explain the low rate of Borrelia detection in the #blood of infected #patients as well as the ability of the #spirochetes to evade the host immune system and resist the antibiotic therapy”: frontiersin.org/articles/10.33…
Here are two images 👉 On the left, a #Borrelia biofilm as seen under a #microscope☝️On the right, a diagram showing how chronic, persister forms of Borrelia can survive inside a #biofilm: where they are better protected from the host immune response: frontiersin.org/articles/10.33… Image
Read 3 tweets
Here, #measles virus #infection caused lymphocyte depletion, with memory T + B cells being most severely affected☝️This #pathogen-driven immunosupppresion supports survival of “co-morbid” infectious agents (polymicrobial disease) nature.com/articles/s4146… ImageImageImage
In fact here, #measles-driven immunosuppression had a prolonged effect on host resistance, extending over 2-3 years science.sciencemag.org/content/348/62… 👉 This suggests measles may promote an atmosphere that favors #microbiome dysbiosis + development of chronic #inflammatory conditions ImageImage
For more on this trend (pathogen-driven immunosuppression + #microbiome dysbiosis) please read this section of my @JCVI book chapter: 👉 “Early #infections predispose a person to later chronic disease” ImageImage
Read 3 tweets

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